Current under-standing of cytomegalovirus infection in immunocompetent individuals

Human cytomegalovirus (CMV) is a member of the herpes family of viruses. Af ter primary infection, it undergoes latency/persistence. Significant progre ss has been made in the last few years in detecting CMV. The most available approach to the diagnosis of CMV infection is the direct detection of CMV antigen in nuclei of peripheral blood leukocytes, an assay known as pp65 di rect antigenemia test. CMV infection is well controlled in the immunocompet ent hosts: however. there are various immunological changes in immune funct ion during and after recovery from CMV infections. Characteristic changes i n lymphocyte subsets occur during CMV infection, mainly involving expansion and activation of CD8 + T lymphocytes and NK cells. On the other hand, CMV has an array of immune escape strategies for establishing a life long late nt state: CMV inhibits: major histocompatibility complex (MHC) class expres sion within infected cells and impairs IFN-gamma-induced MHC class II-depen dent antigen presentation by macrophages; It can also encode proteins that can interfere with the presentation of viral peptide antigens to T cells. W hile cutaneous manifestations of CMV seen in immunocompromised patients hav e been extensively reported, those in adult immunocompetent individuals hav e received relatively little attention: in this setting the primary CMV inf ection appears as CMV mononucleosis. At the time of occurrence of the monon ucleosis syndrome, a variety of extracutaneous and cutaneous manifestations occur. These clinical symptoms are not the direct consequence of prolifera tion of CMV in given tissues but indicative of the immunological response t oward CMV. The incidence of the appearance of eruptions in CMV mononucleosi s is variable. Certain drugs given in the early stage of this disease play an important rule in the development of eruption, just as with the ampicill in rashes in the Epstein-Bari virus mononucleosis. Although the mechanism b y which drugs trigger the development of rashes in patients with CMV mononu cleosis is unknown, it is assumed that CMV is likely to be a potential ampl ifier of drug rashes induced by activation of drug-specific T cells. By imp roving methods for detection of CMV, we can recognize that many types of er uptions other than CMV mononucleosis could be induced by primary infection or reactivation of CMV. (C) 2000 Elsevier Science Ireland Ltd. All rights r eserved.